Abstract
The discovery by Morris et al. (1994) of the genes contributing to the t(2;5)(p23;q35) translocation has laid the foundation for a molecular based recognition of anaplastic large cell lymphoma and highlighted the need for a further stratification of T-cell neoplasia. Likewise the detection of anaplastic lymphoma kinase (ALK) genetic lesions among many human cancers has defined unique subsets of cancer patients, providing new opportunities for innovative therapeutic interventions. The objective of this review is to appraise the molecular mechanisms driving ALK-mediated transformation, and to maintain the neoplastic phenotype. The understanding of these events will allow the design and implementation of novel tailored strategies for a well-defined subset of cancer patients.
Highlights
The concept of anaplastic large cell lymphoma (ALCLs) has changed over the years as a result of a fruitful stream of new information and novel understanding about the cell of origin, biology, genetics, and clinical features of these neoplasms
The discovery of anaplastic lymphoma kinase (ALK) fusion chimera, among ALCLs, has provided the basis for the definition of a unique subgroup among peripheral T-cell lymphoma (PTCL) and set the stage for the identification of new entities, some of which still remain provisional within the current WHO Classification of tumors of hematopoietic and lymphoid tissues
As a matter of fact, we do not know the mechanisms leading to the transformation of ALK− ALCLs, including those involving the skin primarily, or whether various entities among ALCLs somehow share common pathogenetic features and if putative relationship(s) with other T-cell lymphoma may exist
Summary
The discovery by Morris et al (1994) of the genes contributing to the t(2;5)(p23;q35) translocation has laid the foundation for a molecular based recognition of anaplastic large cell lymphoma and highlighted the need for a further stratification of T-cell neoplasia. Likewise the detection of anaplastic lymphoma kinase (ALK) genetic lesions among many human cancers has defined unique subsets of cancer patients, providing new opportunities for innovative therapeutic interventions. The objective of this review is to appraise the molecular mechanisms driving ALK-mediated transformation, and to maintain the neoplastic phenotype. The understanding of these events will allow the design and implementation of novel tailored strategies for a well-defined subset of cancer patients
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